Mitochondrial Fatty Acid Oxidation in Cell Signalling and Energetics

Dear Colleagues,

Fatty acids are essential energetic substrates utilized by oxidative tissues, due to their high carbon content and available free energy. In addition, total or partial fatty acid oxidation provides signaling molecules that allow cells to respond, to adapt, and also, to maladapt to changes in fatty acid levels. Saturated fatty acids constitute a major portion of circulating fatty acids in mammalian systems, but polyunsaturated fatty acids (PUFAs), particularly n-6 PUFAs from soybeans and vegetable oil, and monounsaturated fatty acids (MUFAs) are also abundant. PUFAs are unique in that they can be oxidized via enzyme-mediated and spontaneous reactions; the latter reactions are caused by reactive oxygen (ROS) and nitrogen species (RNS), and typically form lipid peroxides (LOOH) and nitro-fatty acids. These are highly reactive lipid species capable of a variety of biological activities, both beneficial and harmful, including formation of carbonyl-adducts with proteins, phospholipids, and DNA. Particular attention has been directed at the physiological and pathological roles of reactive lipids within mitochondria, an organelle that contains an abundant amount of PUFAs. Another important consequence of lipid metabolism is altered mitochondrial phospholipid composition.
A tight coordination between lipid and mitochondrial metabolism is crucial for avoiding the mitochondrial dysfunction and altered lipid homeostasis typical of a variety of pathological states. Metabolic diseases, such as type 2 diabetes mellitus and obesity, are notably characterized by disruption of normal mitochondrial function and lipid homeostasis. In recent years, it is emerging that other pathologies, including cancer and neurodegeneration, may be driven by metabolic derangements.  For instance, the conversion of normal cells towards a carcinogenic state is accomplished by a reprogramming of metabolic pathways, including mitochondrial and lipid metabolism (e.g., the Warburg effect). Therefore, it is broadly recognized that scientists and physicians require a greater understanding and appreciation for the role of mitochondrial lipid oxidation (enzymatic and spontaneous) in cellular signaling and metabolism under both healthy states and in the occurrence and progression of human pathological states.

Dr. Ethan J. Anderson
Dr. Jacques Robidoux
Guest Editors

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• oxidized lipids as signaling intermediaries regulating the cross-talk between mitochondria and nucleus
• molecular mechanisms involved in metabolic adaptation to nutrient (preferably, but not exclusively, fatty acids) excess or deprivation
• cellular energy demand and mitochondrial lipid oxidation
• dietary lipids and mitochondrial phospholipid composition/oxidation: role of ROS/RNS
• novel and emerging mechanisms regulating lipid catabolism (e.g., lipophagy)
• ros/rns and lipids as regulators of mitochondrial biogenesis
• interplay between mitochondrial lipids and mitophagy
• novel pathways orchestrating mitochondrial fission-fusion dynamics in response to nutrient (preferably, but not exclusively, fatty acids) availability and delivery